A new subtype of frontotemporal lobar degeneration with FUS pathology.

By M. Neumann, Rosa Rademakers, S. Roeber, M. Baker, H. Kretzschmar, I. Mackenzie. Brain : a journal of neurology, 2009

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TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. (2010, background): “Frontotemporal lobar dementia FTLD-TDP-43 Sporadic or familial with or without MND Yes (6,7,43,44,46,47,49, 53–55,57,102,151,267,268, 273–278) No (83,279)”
Phosphorylation of the FUS low‐complexity domain disrupts phase separation, aggregation, and toxicity (2017, unknown): “…of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative diseases, are characterized by neuronal inclusions of the RNA-binding protein fused in sarcoma (FUS; Kwiatkowski et al , 2009; Neumann et al , 2009; Vance et al , 2009; Mitchell et al , 2013).”
The tip of the iceberg: RNA-binding proteins with prion-like domains in neurodegenerative disease (2012, background): “Additional FUS mutations have now also been connected with sporadic ALS and with FTLD-U (Belzil et al., 2009; Blair et al., 2010; Broustal et al., 2010; Corrado et al., 2010; Da Cruz and Cleveland, 2011; DeJesusHernandez et al., 2010; Drepper et al., 2011; Hewitt et al., 2010; Mackenzie et al., 2010”
ALS‐associated fused in sarcoma (FUS) mutations disrupt Transportin‐mediated nuclear import (2010, methodology): “The discovery of TDP-43 and FUS inclusions in both ALS and FTLD has led to the concept that ALS and FTLD are related diseases and that the same proteins are involved in their pathogenesis (Neumann et al, 2009a).”